Li Bai1, Richard T Burnett2, Jeffrey C Kwong3, Perry Hystad4, Aaron van Donkelaar5, Jeffrey R Brook6, Karen Tu7, Ray Copes8, Mark S Goldberg9, Randall V Martin10, Brian J Murray11, Alexander Kopp1, Hong Chen12. 1. Institute for Clinical Evaluative Sciences, Toronto, ON, Canada. 2. Population Studies Division, Health Canada, Ottawa, ON, Canada. 3. Institute for Clinical Evaluative Sciences, Toronto, ON, Canada; Public Health Ontario, Toronto, ON, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada; Department of Family and Community Medicine, University of Toronto, Toronto, ON, Canada. 4. College of Public Health and Human Sciences, Oregon State University, Corvallis, USA. 5. Department of Physics and Atmospheric Science, Dalhousie University, Halifax, NS, Canada. 6. Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada; Air Quality Research Division, Environment and Climate Change Canada, Toronto, ON, Canada. 7. Department of Family and Community Medicine, University of Toronto, Toronto, ON, Canada; Toronto Western Hospital Family Health Team, University Health Network, Canada. 8. Public Health Ontario, Toronto, ON, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada. 9. Department of Medicine, McGill University, Montreal, QC, Canada. 10. Department of Physics and Atmospheric Science, Dalhousie University, Halifax, NS, Canada; Harvard-Smithsonian Center for Astrophysics, Cambridge, MA, USA. 11. Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Canada. 12. Institute for Clinical Evaluative Sciences, Toronto, ON, Canada; Public Health Ontario, Toronto, ON, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada. Electronic address: hong.chen@oahpp.ca.
Abstract
BACKGROUND: Evidence of the adverse neurological effects of exposure to ambient air pollution is emerging, but little is known about its effect on the development of multiple sclerosis (MS), the most common autoimmune disease of the central nervous system. OBJECTIVES: To investigate the associations between MS incidence and long-term exposures to fine particles (PM2.5), nitrogen dioxide (NO2), and ozone (O3) METHODS: We conducted a population-based cohort study to investigate the associations between long-term exposures to PM2.5, NO2, and O3 and the incidence of MS. Our study population included all Canadian-born residents aged 20-40 years who lived in the province of Ontario, Canada from 2001 to 2013. Incident MS was ascertained from a validated registry. We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during the 13 years of follow-up. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for each pollutant separately using random-effects Cox proportional hazards models. We conducted various sensitivity analyses, such as lagging exposure up to 5 years and adjusting for access to neurological care, annual average temperature, and population density. RESULTS: Between 2001 and 2013, we identified 6203 incident cases of MS. The adjusted HR of incident MS was 0.96 (95% CI: 0.86-1.07) for PM2.5, 0.91(95% CI: 0.81-1.02) for NO2, and 1.09 (95% CI: 0.98-1.23) for O3. These results were robust to various sensitivity analyses conducted. CONCLUSIONS: In this large population-based cohort, we did not observe significant associations between MS incidence and long-term exposures to PM2.5, NO2, and O3 in adults in Ontario, 2001-2013. Crown
BACKGROUND: Evidence of the adverse neurological effects of exposure to ambient air pollution is emerging, but little is known about its effect on the development of multiple sclerosis (MS), the most common autoimmune disease of the central nervous system. OBJECTIVES: To investigate the associations between MS incidence and long-term exposures to fine particles (PM2.5), nitrogen dioxide (NO2), and ozone (O3) METHODS: We conducted a population-based cohort study to investigate the associations between long-term exposures to PM2.5, NO2, and O3 and the incidence of MS. Our study population included all Canadian-born residents aged 20-40 years who lived in the province of Ontario, Canada from 2001 to 2013. Incident MS was ascertained from a validated registry. We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during the 13 years of follow-up. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for each pollutant separately using random-effects Cox proportional hazards models. We conducted various sensitivity analyses, such as lagging exposure up to 5 years and adjusting for access to neurological care, annual average temperature, and population density. RESULTS: Between 2001 and 2013, we identified 6203 incident cases of MS. The adjusted HR of incident MS was 0.96 (95% CI: 0.86-1.07) for PM2.5, 0.91(95% CI: 0.81-1.02) for NO2, and 1.09 (95% CI: 0.98-1.23) for O3. These results were robust to various sensitivity analyses conducted. CONCLUSIONS: In this large population-based cohort, we did not observe significant associations between MS incidence and long-term exposures to PM2.5, NO2, and O3 in adults in Ontario, 2001-2013. Crown
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